Diabetes Mellitus is a chronic condition characterized as hyperglycemia (high levels of sugar in blood). Continuing increments of blood glucose levels increase the risk of diabetes-related complications such as kidney damage, vision loss, heart disease, and foot ulcers.
There are two major types of diabetes: type 1 diabetes and type 2 diabetes. With type 1 diabetes, hyperglycemia develops because the pancreas cannot produce insulin. This type of diabetes usually appears in childhood or young adulthood. In type 2 diabetes, the pancreas is capable of producing insulin, but it cannot adequately meet the body's demands. The problem is that the body does not respond to the insulin appropriately, which in turn leads to less glucose being absorbed by the cells and results in abnormally elevated blood glucose levels. After overworking the pancreas for a number of years, the pancreas may eventually fail and exhaust its ability to produce insulin, which at this point a person with type 2 diabetes may require insulin therapy.
Insulin, a natural hormone produced by the pancreas, transports glucose from the bloodstream to the inside of the cells. Thus, the main job of insulin is to regulate the glucose transport into the cells thereby lowering the level of blood glucose.
The actions of insulin are controlled through the activation of a heterotetrameric receptor which is found in the plasma membrane. The insulin receptor is a glycoprotein composed of two extracellular alpha-subunits and two transmembrane beta-subunits linked by disulfide bonds. Ullrich et al., Nature, 313:756-61, 1985. The alpha-subunits contain the insulin-binding domain, and the intracellular portion of the beta-subunit contains the insulin-regulated tyrosine protein kinase (the enzyme that catalyzes the transfer of a high-energy group from a donor (usually ATP) to an acceptor).
When an insulin molecule is released by the beta cells of the pancreas and arrives at a cell, it binds onto the insulin receptor on the surface of most cells. Once insulin binds, the intrinsic phosphotransferase function of the insulin receptor beta-subunit is activated, resulting in the tyrosine phosphorylation of a number of intracellular proteins. Once the insulin receptor has been activated, the phosphorylation event leads to an increase in glucose storage and consequently a decrease in blood glucose levels.
Effective control of glucose level is difficult to achieve for prolonged periods even with the most meticulous mode of insulin therapy in the most motivated patients. Thus, there is a continuing need for new drug products with desired therapeutic efficacy for treatment of diseases and metabolic disorders.
Nitric oxide (NO) is a gaseous molecule that has been shown to acts in the signaling of different biological processes. Endothelium-derived NO is a key molecule in regulation of vascular tone and its association with vascular disease has long been recognized. NO inhibits many processes known to be involved in the formation of atherosclerotic plaque, including monocyte adhesion, platelet aggregation and vascular smooth muscle cell proliferation. Another important role of endothelial NO is the protection of the vascular wall from the oxidative stress induced by its own metabolic products and by the oxidation products of lipids and lipoproteins. Endothelial dysfunction occurs at very early stages of atherosclerosis. It is therefore possible that deficiency in local NO availability could be a final common pathway that accelerates atherogenesis in humans. In addition to its role in the vascular endothelium, NO availability has been shown to modulate metabolism of lipoproteins. Negative correlation has been reported between plasma concentrations of NO metabolic products and plasma total and Low Density Lipoprotein [LDL] cholesterol levels while High Density Lipoprotein [HDL] improves vascular function in hypercholesterolaemic subjects. The loss of NO has considerable effect on the development of the disease. Diabetes mellitus is associated with increased rates of morbidity and mortality caused primarily by the accelerated development of atherosclerotic disease. Moreover, reports show that diabetics have impaired lung functions. It has been proposed that insulin resistance leads to airway inflammation. Habib et al., Nitric Oxide Measurement From Blood To Lungs, Is There A Link? Pak J Physiol 2007; 3(1).
Nitric oxide is synthesized by the endothelium from L-arginine by nitric oxide synthase (NO synthase). NO synthase occurs in different isoforms, including a constitutive form (cNOS) and an inducible form (iNOS). The constitutive form is present in normal endothelial cells, neurons and some other tissues.
The therapeutic effect of an extremely diluted (or ultra-low) form of antibodies potentized by homeopathic technology has been discovered by the inventor of the present patent application, Dr. Oleg I. Epshtein. U.S. Pat. No. 7,582,294 discloses a medicament for treating Benign Prostatic Hyperplasia or prostatitis by administration of a homeopathically activated form of antibodies to prostate specific antigen (PSA). U.S. Pat. No. 7,700,096 discloses a homeopathically potentized form of antibodies to endothelial NO-synthase. The homepathically potentized form of antibodies to endothelial NO-synthase is marketed in the Russian Federation and other countries under the name IMPAZA®.